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Chronic Inflammation and γδ T Cells.
Fay, Nathan S; Larson, Emily C; Jameson, Julie M.
Affiliation
  • Fay NS; Department of Biological Sciences, California State University, San Marcos , San Marcos, CA , USA.
  • Larson EC; Department of Biological Sciences, California State University, San Marcos , San Marcos, CA , USA.
  • Jameson JM; Department of Biological Sciences, California State University, San Marcos , San Marcos, CA , USA.
Front Immunol ; 7: 210, 2016.
Article in En | MEDLINE | ID: mdl-27303404
The epithelial tissues of the skin, lungs, reproductive tract, and intestines are the largest physical barriers the body has to protect against infection. Epithelial tissues are woven with a matrix of immune cells programed to mobilize the host innate and adaptive immune responses. Included among these immune cells are gamma delta T lymphocytes (γδ T cells) that are unique in their T cell receptor usage, location, and functions in the body. Stress reception by γδ T cells as a result of traumatic epithelial injury, malignancy, and/or infection induces γδ T cell activation. Once activated, γδ T cells function to repair tissue, induce inflammation, recruit leukocytes, and lyse cells. Many of these functions are mediated via the production of cytokines and growth factors upon γδ T cell activation. Pathogenesis of many chronic inflammatory diseases involves γδ T cells; some of which are exacerbated by their presence, while others are improved. γδ T cells require a delicate balance between their need for acute inflammatory mediators to function normally and the detrimental impact imparted by chronic inflammation. This review will focus on the recent progress made in understanding how epithelial γδ T cells influence the pathogenesis of chronic inflammatory diseases and how a balance between acute and chronic inflammation impacts γδ T cell function. Future studies will be important to understand how this balance is achieved.
Key words

Full text: 1 Collection: 01-internacional Database: MEDLINE Language: En Journal: Front Immunol Year: 2016 Document type: Article Affiliation country: United States Country of publication: Switzerland

Full text: 1 Collection: 01-internacional Database: MEDLINE Language: En Journal: Front Immunol Year: 2016 Document type: Article Affiliation country: United States Country of publication: Switzerland